JC polyomavirus (JCV or JCPyV) is a non-enveloped DNA virus that chronically infects the urinary tract of most adults. Although JCV is not known to cause noticeable symptoms in healthy subjects, the virus can cause a lethal brain disease, progressive multifocal leukoencephalopathy (PML), in immunosuppressed individuals. The incidence of JCV-induced PML increased dramatically during the AIDS epidemic, affecting roughly 1-3% of human immunodeficiency virus (HIV) seropositive individuals (Major, Cleve. Clin. J. Med. 78(Suppl 2):53-7, 2011). The availability of highly active antiretroviral therapy (HAART) has dramatically reduced the lethality of PML; however, its debilitating symptoms remain a significant risk for HIV-infected individuals (Simpson, Cleve. Clin. J. Med. 78(Suppl 2):524-27, 2011).
In recent years, JCV-induced PML has increasingly been found in patients treated with immunosuppressive drugs, including a variety of new monoclonal antibody therapeutics such as natalizumab and rituximab (Weissert, J. Neuroimmunol. 231:73077, 2011; Novak et al., Arch. Neurol. 65:1162-1165, 2008; Major, N. Engl. J. Med. 361:1041-1043, 2009; Major, Ann. Rev. Med. 61:35-47, 2010). An apparent common feature of HIV infection and PML-associated immunosuppressive therapies is the induction of decreased cell-mediated immunity within the central nervous system (CNS). Decreased T cell surveillance presumably allows JCV to emerge from latency and initiate a spreading infection within the CNS (Gheuens et al., Ann. Rev. Pathol. 8:189-215, 2013). Recent reports have found a unique spectrum of mutations in the VP1 gene of JCV strains found in PML patients (Gorelik et al., J. Infect. Dis. 204:103-114, 2011; Reid et al., J. Infect. Dis. 204:237-244, 2011), leading to speculation that the VP1 mutations might be involved in PML pathogenesis. The VP1 mutations associated with PML are not detected in urine (where JCV is typically shed); thus, JCV sequences found in urine are defined in the field as “wild-type.” There remains a need for compositions and methods to prevent or inhibit JCV infection or the development of PML (or both) in vulnerable subjects.